Long working hours associated with an increased risk for atrial fibrillation

Long working hours as a risk factor for atrial fibrillation: a multi-cohort study

Background

Psychosocial stress at work is a potential risk factor for CVD. It may enhance functional re-entry, repetitive pulmonary vein and atrial firing, as well as autonomic nervous system abnormalities, inducing arrhythmia vulnerability [1-3]. Evidence from small study samples suggest that stress and ‘exhaustion’ predict symptomatic AF. In the present large-scale study, the association between long working hours and incident AF was evaluated in the general population, using data from cohort studies participating in the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium [4-6].

The following 8 studies were designed to examine health effects across a range of risk factors, including those related to workplace: the Copenhagen Psychosocial Questionnaire Study (COPSOQ) I and COPSOQ-II, the Danish Work Environment Cohort Study (DWECS), the Finnish Public Sector Study (FPS), the Health and Social Support study (HeSSup), the PUMA study, the Whitehall II study and the Work, Lipids and Fibrinogen study (WOLF).

These studies included 85 494 participants who were free of AF at baseline. Participants with any indication of pre-existing AF in electronic health records or ECG at baseline were excluded (n=250).

Working hours were assessed at baseline, between 1991 and 2004, and classified into the following categories: <35 h (part-time), 35–40 h (standard working hours, reference group), 41–48 h (above average, but still in line with the EU Working Time Directive), 49–54 h , ≥55 h/week (most commonly used threshold for working long hours in medical research).

Main results

During an average follow-up of 10 years, there were 1061 incident AF events.

After adjustment for age, gender and socioeconomic status, participants working long hours (>55hrs) were at increased risk of incident AF: the HR compared with those working standard hours is 1.42 (95% CI: 1.13–1.80; P= 0.0031). There was little heterogeneity in the cohort-specific estimates (I2 = 0%; P= 0.66).

The association between long working hours and AF was maintained after adjustment for pre-existing CHD at the time of AF diagnosis (HR: 1.41; 95% CI: 1.12–1.78; P= 0.0039) and after excluding participants with CVD at baseline (N= 549; HR: 1.41; 95% CI: 1.11–1.79; P= 0.0054) or CVD at baseline or follow-up (N= 2006; HR: 1.36; 95% CI: 1.05–1.76; P= 0.0180).

There was a dose-response gradient with HRs of 1.02, 1.17, and 1.42 for 41–48, 49–54 and ≥ 55 working hours per week compared with standard working hours per week.

In stratified analyses, the association between long working hours and AF did not differ between men and women (P=0.267), participants younger than 50 and those 50 years or older at baseline (P= 0.704) or by socioeconomic group (P=0.186).

Conclusion

In a large-scale meta-analysis, participants working over 55 hours per week were 40% more likely to develop AF compared with those working standard hours. This association was independent of known AF risk factors.

Editorial comment

In their editorial article, Mahmoodi and Boersma summarize the results of the Kivimaki et al study, and note: ‘It is worth noting that the individual studies were all underpowered to detect statistically significant associations; the authors should be congratulated for the impressive collaborative effort required to integrate patient-level data from multiple studies to increase the power.’

They also point out the study limitations, the most important being:

Possible changes regarding the working hours and the adjustment variables during the long follow-up period are lacking.

Other potential confounders, like the kind of work, expanding from office jobs to jobs that are physically demanding, or irregular working hours, including night shifts, are not taken into account.

The authors conclude: ‘Although the results of the present study apparently identify an association between working hours and AF, whether the relationship is causal or not remains to be determined. The results provide no insight into the mechanism by which working hours may affect the heart leading to development of AF. Intuitively, one would suspect the usual pathways causing changes in autonomic tone and increasing atrial fibrosis resulting in AF, but no evidence yet exists to prove such a mechanism.’